Analgesic Nephropathy
| Overview |
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- Analgesic Nephropathy refers to a chronic inflammation of the renal interstitium arising from long-term simultaneous use of phenacetin and aspirin.
| Pathogenesis |
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- Overview
- The pathogenesis of analgesic nephropathy is not well-understood but appears to arise from combined use of both phenacetin and aspirin which synergize to result in renal interstitial damage.
- Phenacetin:
- Phenacetin appears to concentrate in the renal medulla and result in tissue injury possibly by generation of rree radicals or direct binding to tubular proteins.
- Aspirin:
- Recall that prostoglandins are important for maintaining blood flow through the kidneys by maintaining vasodilation of the renal afferent and efferent arterioles (See: Neuroendocrine Regulation of GFR and RBF). Aspirin reduces prostoglandin synthesis and thus causes vasoconstriction of the afferent and efferent arterioles, thus rendering the poorly perfused renal medulla highly prone to injury by phenacetin.
| Morphology |
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- The proximate pathological consequence of analgesic nephropathy appears to be necrotizing papillitis of the renal papillae. Further interstital inflammation observed in patients likely occurs as a response to the necrotizing papillitis.
| Clinical Consequences |
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- Analgesic Nephropathy can progress to chronic renal failure if not corrected.